ArticleThe Journal of biological chemistry2020
Tafazzin deficiency impairs CoA-dependent oxidative metabolism in cardiac mitochondria.
Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Peroxisomal catalase and plasmalogen biosynthesis protect from oxidative stress in Barth syndrome cardiomyopathy.Basic research in cardiology · 2026Article
- Article
- Cardiolipin remodelling in mitochondrial therapeutics: translational evidence chains from elamipretide to emerging strategies.Frontiers in physiology · 2026Review
- Article
- Tafazzin-deficient zebrafish display mitochondrial dysfunction, neutropenia, and metabolic defects without myopathy.Scientific reports · 2025Article
- A murine model of Barth syndrome recapitulates human cardiac and skeletal muscle phenotypes.Disease models & mechanisms · 2025Article
- Barth Syndrome:Genes · 2025Review
- Activation of the integrated stress response rewires cardiac metabolism in Barth syndrome.Basic research in cardiology · 2023Article
- Metabolic switch from fatty acid oxidation to glycolysis in knock-in mouse model of Barth syndrome.EMBO molecular medicine · 2023Article
- Single Cell Transcriptomic Analysis in a Mouse Model of Barth Syndrome Reveals Cell-Specific Alterations in Gene Expression and Intercellular Communication.International journal of molecular sciences · 2023Article
- The Key Role of Mitochondrial Function in Health and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Elevated liver glycogenolysis mediates higher blood glucose during acute exercise in Barth syndrome.PloS one · 2023Article
- Article
- Mechanical characterization of isolated mitochondria under conditions of oxidative stress.Biomicrofluidics · 2022Article
- Beneficial effects of SS-31 peptide on cardiac mitochondrial dysfunction in tafazzin knockdown mice.Scientific reports · 2022Article
- Barth Syndrome Cardiomyopathy: An Update.Genes · 2022Review
- Stimulating myocardial pyruvate dehydrogenase activity fails to alleviate cardiac abnormalities in a mouse model of human Barth syndrome.Frontiers in cardiovascular medicine · 2022Article
- Myocardial disturbances of intermediary metabolism in Barth syndrome.Frontiers in cardiovascular medicine · 2022Review
- Chronic Lactate Exposure Decreases Mitochondrial Function by Inhibition of Fatty Acid Uptake and Cardiolipin Alterations in Neonatal Rat Cardiomyocytes.Frontiers in nutrition · 2022Article
- Skeletal Muscle Mitochondria Dysfunction in Genetic Neuromuscular Disorders with Cardiac Phenotype.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Barth syndrome is a mitochondrial myopathy resulting from mutations in the tafazzin (
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.